Right ventricular failure may be defined as the inability of the right ventricle of the heart to provide adequate blood flow through the pulmonary circulation at a normal central venous pressure. Critical care specialists encounter right ventricular failure routinely in their practice, but until recently right ventricular failure as a primary clinical entity received scant consideration. Indeed, there is still not a single published practice guideline focused on right ventricular failure. Right ventricular failure is usually due to a combination of right ventricular pressure overload and contractile abnormalities of the right ventricular free wall. Decompensation may occur abruptly and catastrophically because of unique aspects of right ventricular physiology. This review will focus on the pathophysiology of acute right ventricular failure in the critical care setting and summarize the limited management options available.

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Heightened cardiovascular risk among patients with systemic insulin resistance is not fully explained by the extent of atherosclerosis. It is unknown whether myocardial insulin resistance accompanies systemic insulin resistance and contributes to increased cardiovascular risk. This study utilized a porcine model of diet-induced obesity to determine if myocardial insulin resistance develops in parallel with systemic insulin resistance and investigated potential mechanisms for such changes. Micropigs (n = 16) were assigned to control (low fat, no added sugars) or intervention (25% wt/wt coconut oil and 20% high-fructose corn syrup) diet for 7 mo. Intervention diet resulted in obesity, hypertension, and dyslipidemia. Systemic insulin resistance was manifest by elevated fasting glucose and insulin, abnormal response to intravenous glucose tolerance testing, and blunted skeletal muscle phosphatidylinositol-3-kinase (PI 3-kinase) activation and protein kinase B (Akt) phosphorylation in response to insulin. In myocardium, insulin-stimulated glucose uptake, PI 3-kinase activation, and Akt phosphorylation were also blunted in the intervention diet group. These findings were explained by increased myocardial content of p85alpha (regulatory subunit of PI 3-kinase), diminished association of PI 3-kinase with insulin receptor substrate (IRS)-1 in response to insulin, and increased serine-307 phosphorylation of IRS-1. Thus, in a porcine model of diet-induced obesity that recapitulates many characteristics of insulin-resistant patients, myocardial insulin resistance develops along with systemic insulin resistance and is associated with multiple abnormalities of insulin signaling.